In the rat brain, global hypoxia cause a delayed neuronal degeneration that occurs hours to days after reoxygenation. It is generally thought that the ischemic damage is initiated by neurotoxicity mediated through glutamate receptors, particulary NMDA subtypes. Calcium entry through the NMDA receptor is responsible for the synaptic plasiticity and neuronal pathology. Degradation of MAP-2 and NF200, a major components of neuronal cytoskeleton, by Ca2+-dependent protease after NMDA receptor activation has been postulated in delayed neuronal damage. Changes of NR subunit 2B, MAP2 and NF200 in rat brain postsynaptic density[PSD] after hypoxic injury were investigated through immunoblot analyses. To understand the effect of Ca2+ influx through NMDA receptors on neuronal damage which is manifested by cytoskeletal disruption, morphological change was examined through immunohistochemistry and H & E staining. We found that immunoreactivity to NR2B antibody in the cerebral cortex PSD was up-regulated while MAP2 and NF200 was down-regulated at 30 hours after initial hypoxic insult. At this time, morphological changes of neuronal cells in hypoxic conditions were manifested as down-regulation of MAP2 and NF200 immunoreactivities, hyperchromatic condensation of cytoplasm and nucleus, homogenizing cell change, expansion of perineuronal space and dispersion of chromatin. From 3 days, NR2B, MAP2, NF200 were up-regulated simultaneously. On the other hand, morphological alterations in hypoxic neurons were progress further. Our present results suggests that Calcium influx through NR1/NR2B receptor channel is effective whithin 30 hours but ineffective from 30 hours. Delayed neuronal cell death triggered by Ca2+ influx through NR1/NR2B receptor channel within 30 hours, which may activate intracellular profeases. Proteolysis of cytoskeleton by activated protease leads to its abnormal reorganization and eventually damages normal function of cell membrane which causes neuronal cell death.
Animals ; Anoxia ; Brain ; Calcium ; Cell Death ; Cell Membrane ; Cerebral Cortex* ; Chromatin ; Cytoplasm ; Cytoskeleton* ; Down-Regulation ; Hand ; Immunohistochemistry ; N-Methylaspartate* ; Neurons ; Pathology ; Proteolysis ; Rats* ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate ; Up-Regulation*

Transient cerebral ischemia was induced by bilateral common carotid artery ligation with reperfusion to understand its effect on the expression of NMDA receptor subunits 2A (NR2A), 2B (NR2B), and NF200 The changes of the expressions of NR2A, NR2B, and NF200 in cerebral postsynaptic density (PSD) were evaluated through immunoblot analyses. The expressions of NR2A and NF200 were markedly decreased until 18 hours after reperfusion, while that of NR2B was increased. The immunohistochemistry with NFIGO antibody showed that NF200 protein, which is a marker for neuronal damage, was also significantly decreased at this time point indicating neuronal damages, and the morphological damages of neuronal cells were evident by hyperchromatic condensation of nucleus, irregular cell membrane, displacement of nucleus, and chromatolysis of Nissl substances in toluidine blue stain. However, from 18 hours to 3 day after reperfusion, immunoblot analyses showed that NF200 was increased significantly, while the expression of NR2A were recovered to the control level and that of NR2B was returned to somewhat higher level than control. The NR1/NR2B-type receptor is known to have a longer offset decay time than NR1/NR2A-type ones, and to be more potent in Ca2 influxing. Therefore, our results suggest that, until 18 hours, neurons are damaged by overinflux of Ca2 through NR1/NR2B receptors which helps to degrade NF200 by Ca2 sensitive professes resulting in damages to intracellular transport. The fact that the expression of NF200 was increased even though the NR2A and NR2B are control level during 18 hours to 3 days after damage suggests that NMDA receptor subunits expressed at this time may not form functional receptors. The worsening of some neuronal damages after 3 days may indicate that an abnormal reorganization of elevated NF200 between 18 hours to 3 days further disturb intracellular transport and functions of cell membrane which cause cell death.
Animals ; Carotid Artery, Common ; Cell Death ; Cell Membrane ; Cerebral Cortex* ; Immunohistochemistry ; Ischemic Attack, Transient* ; Ligation ; N-Methylaspartate* ; Neurons ; Post-Synaptic Density ; Rats* ; Reperfusion ; Tolonium Chloride

In the rat brain, partial ischemia causes a delayed neuronal degeneration that occurs hours to days after reoxygenation. It is generally thought that the ischemic damage is initiated by neurotoxicity mediated through glutamate receptors, particulaly NMDA subtypes. Calcium entry through the NMDA receptor is responsible for the synaptic plasiticity and neuronal pathology. Degradation of MAP-2 and NF200, a major components of neuronal cytoskeleton, by Ca2+-dependent protease after NMDA receptor activation has been postulated in delayed neuronal damage. Calcium-activated protease calpain, excessive degradation of MAP-2, together with the calpain-sensitive microtubule and neurofilaments, would be expected to disrupt intracellular transport- and membrane-related functions that is vital to neurons. Changed of NR subunit 2A, 2B, MAP2 and NF200 in rat hippncampal postsynaptic density[PSD] after partial ischemic injury were investigated though immunoblot analyses. To understand the effect of Ca2+, influx through NMDA receptors on neuronal damage which is manifested by cytoskeletal disruption, morphological change was examined through immunohistochemistry and routine staining method. We found that immunoreactivity to NR2B receptor subuit in the hippocampal formation PSD was upregulated while MAP2 and NF200 was down-regulted at 18 hours after initial partial ischemic insult. On the other hand, morphological changes of neuronal cell in partial ischemic conditions were manifested as eosinophilic inclusion bodies in the cytoplasm which is progression of neuronal damage after 6 days. Calcium influx through NR1/NR2B receptor channel may activate intracellular proteases which would degrade cytoskeleton. Proteolysis of cytoskeleton leads to its reorganization and eventually damages normal function of cell membrane which cause neuronal cell death.
Animals ; Brain ; Calcium ; Calpain ; Cell Death ; Cell Membrane ; Cytoplasm ; Cytoskeleton ; Eosinophils ; Hand ; Hippocampus* ; Immunohistochemistry ; Inclusion Bodies ; Ischemia ; Microtubules ; N-Methylaspartate ; Neurons ; Pathology ; Peptide Hydrolases ; Proteolysis* ; Rats* ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate

Congenital radial clubhand is a rare deformity, which is characterized by total or partial absence of the radial ray of forearm and hand. We experienced 9 radial clubhands in 7 patients during the last 12 years. Excluding 3 clubhands in 2 patients which were very mild in their deformity, 6 clubhands in 5 patients were operated. Radialization was done in 5 clubhands, and centralization in one. Concomitant corrective osteotomy of ulna was combined in all. The results of the surgical treatment were evaluated by ; radiological findings including Hand-forearm angle(HFA), Hand-forearm position(HFP) and Ulnar bowing(UB) range of motion of the wrist ; and parents' satisfaction. Patients were followed up for average 2 years and 6 months, ranging from 1 to 6 years. All the radiological findings were improved. Although their range of wrist motion was not increased, this was changed into more functional position, that is the radial deviation decreased but ulnar deviation increased. Most parents were satisfied with the surgical results.
Congenital Abnormalities ; Forearm ; Hand ; Humans ; Osteotomy ; Parents ; Range of Motion, Articular ; Ulna ; Wrist

Azithromycin* ; Doxycycline* ; Scrub Typhus*

There has been a few articles dealing with the incidence of congenital anomalies of the hand in Korea. In this paper, we have analyzed patients who have visited the hand clinic of Seoul National University Children s Hospital from March 1993 to February 1995 to study the relative incidence of congenital anomalies of the hand. We regarded more than two visits of the same patients as one. They were categorized into two groups by our classification system. First group consisted of the patients who showed hand anomaly only. The other group consisted of the patients who had anomalies in the other sites as well as in the hand. The first group was divided into two subgroups; the patients who had single entity of hand anomaly, and those who had more than two entities of hand anomalies. From the clinical analysis based on above criteria, following results were obtained. There were 626 anomalies in 547 patients, 319 (58.3%) males and 228 (41.7%) females (1.4: 1). Unilateral involvements of hand anomaly were noted in 385 (70.3%) patients (229 in right, 156 in left) and bilateral in 162 (29.7%). As a whole, the most common anomaly was trigger thumb (16.5%) and the second was polydactyly (16.1%). Other anomalies, in order of frequency, were syndactyly, camptodactyly, hypoplasia, brachydactyly, cleft hand and so on. In the first group who had hand anomaly only, there were 407 patients who had single entity of hand anomaly. Among these, trigger thumb were 25.3%, and polydactyly 16.2%. There were 68 patients who had multiple entities of anomalies. Among these, the syndactyly was the most common anomaly (23.9%) and the polydactyly was the next (16.2%). Fifty eight (10.6%) patients had anomalies in the hand as well as in the other site. Among these, camptodactyly was the most commonly found (36.5%) and polydactyly was the next common variety (19.0%) in the hand. In the anomalies which occurred in other than hand, arthrogryposis multiplex congenita was the most common (30.0%). Syndactyly of the foot (22.9%) and polydactyly of the foot (18.6%) were the next common anomalies.
Arthrogryposis ; Brachydactyly ; Child ; Classification ; Female ; Foot ; Hand* ; Humans ; Incidence* ; Korea ; Male ; Polydactyly ; Seoul ; Syndactyly ; Trigger Finger Disorder

Collagen is the major structural protein in the human body, especially in connective tissues. There are more than 13 types of collagen. Among them, type II collagen is a main component of articular cartilage structure. Altered immunological conditions against type II collagen may be closely related to the pathologic conditions of joint, especially arthritis. Since 1977, animal model for collageninduced arthritis(CIA) has been developed and used in the investigation of arthritis. In those animals, high titers of anti-type II collagen antibody were noticed. Pathologic findings were similar to rheumatoid arthritis of human, which suggested that rheumatoid arthritis might be one of the autoimmune diseases. There had been many reports about elevation of serum and synovial level of anti-type II collagen antibody in rheumatoid arthritis patients. But majority of them did not discriminate the antibody titers according to the type of immunoglobulin(i.e. IgG, IgM). And the question whether the elevated antibody titers are cause or effect of the arthritis is still in controversy. In this study, the serum levels of anti-type II collagen antibody were determined in 82 persons(35 degenerative arthritis patients, 24 rheumatoid arthritis patients and 22 normal controls without any joint problem) via ELISA method. In each person the serum IgG, IgM and IgG+M+A antibody levels against bovine type IIcollagen and chicken typeII collagen were determined individually. Statistical evaluation of these data among degenerative arthritis group, rheumatoid arthritis group and normal control group was performed. The results were as follows; 1. Degenerative arthritis group revealed significant elevation of anti-type II collagen antibody(IgG, IgG+M+A) compared to normal control(p < 0.05). 2. Rheumatoid arthritis group showed significant elvation of IgM and IgG+M+A compared to normal control. 3. Between degenerative arthritis and rheumatoid arthritis group, no sigificant difference was noticed. 4. Rheumatoid arthritis group showed significant increase of IgM antibody level compared to normal control. 5. Female rheumatoid arthritis group showed significant increase of IgM level compared to female degenerative arthritis group. These findings suggested that the elevation of anti-type II collagen antibody titer is not specific for rheumatoid arthritis and related with general pathologies destroying articular cartilage. And it is suggested that anti-type II collagen antibody associated with rheumatoid arthritis is mainly IgM proportion, especially in female patients. So further investigation of anti-type II collagen antibody associated with rheumatoid arthritis is needed to target IgM antibody.
Animals ; Arthritis ; Arthritis, Rheumatoid ; Autoimmune Diseases ; Cartilage, Articular ; Chickens ; Collagen ; Collagen Type II ; Connective Tissue ; Enzyme-Linked Immunosorbent Assay ; Female ; Human Body ; Humans ; Immunoglobulin G ; Immunoglobulin M ; Joints ; Methods ; Models, Animal ; Osteoarthritis ; Pathology

No abstract available.
Gonadotropin-Releasing Hormone* ; Gonadotropins*

We describe a case of cutaneous angiomyolipoma found in the ear lobe, that is not associated with tuberous sclerosis. The lesion developed on the youngest patient yet reported in the literature.
Angiomyolipoma* ; Ear ; Humans ; Tuberous Sclerosis

This study was conducted to evaluate the effect of PTSD on memory funtion and hippocampal volume, and to identify major variables correlated to hippocampal volume and memory function. Thirty four Vietnam veterans were collected for this study, among whom eighteen were PTSD patients and sixteen were combat control subjects. The author used Impact of Event Scale(IES), Combat Exposure Scale(CES), Hamilton Depression Rating Scale(HDRS) and Beck Depression Inventory(BDI). Korea Memory Assessment Scale(K-MAS) was assessed for memory function. Magnetic resonance imaging(MRI) was used to measure hippocampal volume. There were significant differences between PTSD and Non-PTSD veterans in IES, HDRS and BDI. Significant difference was found in verbal memory and total memory of K-MAS between PTSD and Non-PTSD veterans. There was significant difference in hippocampal volume between PTSD and Non-PTSD veterans. Short term memory, verbal memory and total memory were positively correlated to hippocampal volume. Hippocampal volume was negatively correlated to IES, HDRS, and BDI. These results suggest that PTSD severity be associated with hippocampal atrophy and memory dysfunction. Reduced or smaller hippocampal volume may be preexisting risk factor for stress exposure or the development of PTSD on combat exposure.
Atrophy ; Depression ; Hippocampus ; Humans ; Korea ; Memory* ; Risk Factors ; Stress Disorders, Post-Traumatic* ; Veterans ; Vietnam